Advancing Knowledge. Enhancing Care.
Advancing Knowledge. Enhancing Care.

Psoriasis News

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EADV 2020 | Targeting IL17 and IL23

Biologics 2020

Presented by Curdin Conrad, MD

A report from the 29th Congress of the European Academy of Dermatology and Venereology

The IL-17 and IL-23 targeting biologics have transformed psoriasis management and continue to set new standards in cutaneous clearance, durable response, and safety.

IL-17 blockade demonstrates excellent PASI response across many trials, and response is quite long-lasting. Secukinumab achieves exceptional PASI-90/100 response (76.2% and 45.9%) through 52 weeks, and results are similar for other IL-17 drugs.14 Early selection of appropriate IL-17 agents is also vital for drug survival. Egeberg, et al., showed that more than 80% of bionaive patients remain on secukinumab after 3 years, compared to only 50% and 33% with one or two plus prior biologics, respectively.15

Anti-IL-23p19 drugs have pushed clearance even further. For example, risankizumab demonstrated PASI-100 response in 58% in both treatment and placebo crossover arms.16 Another major benefit of the IL-23 blockade is sustained and apparent disease-altering response approaching 6 months, which is considerably longer time than the half-life of these drugs.

When choosing between classes, some factors should be considered. Though the anti-IL-23p19 drugs have higher response rates, ixekizumab and secukinumab (IL-17) both exhibit more rapid clearance than guselkumab (IL-23p19) across the first 20 weeks.17,18 Additionally, IL-17 blockade shows considerable promise in psoriatic arthritis (PsA), with ACR50 arthritis improvement equivalent or superior to adalimumab in some trials.19,20

A major reason for choosing against IL-17 drugs is inflammatory bowel disease (IBD). IBD unmasking or flare occurs as anti-IL-17 targets both subsets of Th17 cells, the pathogenic (inflammation, due to IL-17 and IL-22) and non-pathogenic (barrier function, due to IL-17 and IL-10). The IL-23 therapies block only stimulation of pathogenic T-cells, reducing inflammation but sparing some IL-17 for intestinal barrier repair and flora control.21,22



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